Norovirus Gastroenteritis, Carbohydrate Receptors, and Animal Models

Division of Infectious Diseases, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America.
PLoS Pathogens (Impact Factor: 8.06). 08/2010; 6(8):e1000983. DOI: 10.1371/journal.ppat.1000983
Source: PubMed
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    • "ORF2 is approximately 1.8 kb and encodes the 57 kDa major capsid protein, VP1, while ORF3 is approximately 0.6 kb and encodes a 33 kDa minor structural protein, VP2 (McFadden et al., 2011). VP1 is suggested to be involved in the recognition of the host cell receptor (Tan & Jiang, 2010) while VP2 is thought to be involved in the stability of the capsid but also seems to be vital for viral assembly (Glass et al., 2009). Recent studies have shown that murine norovirus has an additional ORF, ORF4, which overlaps ORF2 in an alternate reading frame (Thackray et al., 2007). "
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    ABSTRACT: Diarrhea is considered to be the second leading cause of death due to infections among children <5 years of age worldwide that may be caused by bacteria, parasites, viruses and non-infectious agents. The major causative agents of diarrhea in developing countries may vary from those in developed countries. Noroviruses are considered to be the most common cause of acute diarrhea in both children and adults in industrialized countries. On the other hand, there is lack of comprehensive epidemiological evidence from developing countries that norovirus is a major cause of diarrhea. In these regions, asymptomatic norovirus infections are very common, and similar detection rates have been observed in patients with diarrhea and asymptomatic persons. This review summarizes current knowledge of norovirus infection in developing countries and seeks to position infections with noroviruses among other enteropathogens as disease burden in these regions.
    Journal of General Virology 05/2015; DOI:10.1099/vir.0.000194 · 3.53 Impact Factor
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    • ". ORF2 and ORF3 encode a viral capsid protein (VP1) and a minor capsid protein (VP2), respectively, the latter of which serves to stabilize VP1 [Jiang et al., 1993]. The functional domain of NoV VP1 is composed of a shell (S) and two protruding (P) domains, P1 and P2 [Tan et al., 2003; Lindesmith et al., 2008; Tan and Jiang, 2010]. The S and P1 domains are relatively conserved within a given genotype of NoV. "
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    ABSTRACT: The incidence of noroviral gastroenteritis has increased dramatically in recent years, and norovirus (NoV) genogroup II.4 (GII.4) is associated with outbreaks worldwide. The NoV genotypes and their clinical relevance in children hospitalized with acute gastroenteritis between 2006 and 2011 in northern Taiwan were evaluated in this study. NoV sequences were amplified from 47 clinical specimens and phylogenetic analysis was performed. Based on noroviral capsid protein (VP1) and RNA dependent RNA polymerase (RdRp) phylogeny, circulating NoV could be divided into GII.2, GII.3, GII.12, and GII.4 and GII.16, GII.12, GII.g, and GII.4; respectively. The GII.4 subtype was predominant and could be divided further into the 2004 (Hunter), 2006b, and 2010 (New Orleans) subtypes. Regarding clinical manifestations, convulsive disorder occurred only in cases caused by NoV GII.4 2006b. Patients affected by NoV GII.4 2006b presented with a higher frequency of diarrhea (P = 0.0204), longer duration of diarrhea (P = 0.0215), more frequent hypoglycemia (P = 0.038), and electrolyte imbalance (P = 0.0487) than acute gastroenteritis caused by NoV GII.4 2010. Structural analysis showed that the amino acid changes in viral VP1 between GII.4 2006b and 2010 subtype were located mainly in the protruding domain 2 (P2 domain). In conclusion, the NoV GII.4 variants 2006b and 2010 were the main causes of acute gastroenteritis in hospitalized children in northern Taiwan during 2006-2011. The clinical presentations and structural changes in VP1 of the two NoV GII.4 variants should be evaluated in the future. J. Med. Virol. © 2013 Wiley Periodicals, Inc.
    Journal of Medical Virology 02/2014; 86(2). DOI:10.1002/jmv.23728 · 2.22 Impact Factor
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    • "A decade after FCV first came on the scene, Wobus et al. (2006) identified murine norovirus-1 (MNV) as a closer genetic relative of NoV. Now, MNV has become the more commonly used surrogate for chemical disinfection studies (Belliot et al. 2008; Cannon et al. 2006; D'Souza and Su 2010; Lee et al. 2008; Lim et al. 2010; Magulski et al. 2009; Park et al. 2010; Sattar et al. 2011); and studies on processing interventions like heating (Baert et al. 2008a; Cannon et al. 2006; Hewitt et al. 2009; Sow et al. 2011; Tanner 2009), freezing (Baert et al. 2008b), UV irradiation (Jean et al. 2011; Park et al. 2011), gamma irradiation (Feng et al. 2011), electron beam (Sanglay et al. 2011), and high pressure processing (Kingsley et al. 2007; Lou et al. 2011; Tang et al. 2010). Poliovirus and bacteriophage MS2 have also been used as potential surrogates for NoV (Bae and Schwab 2008; D'Souza and Su 2010; Dawson et al. 2005; Shin and Sobsey 2003). "
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    ABSTRACT: The inability to propagate human norovirus (NoV) or to clearly differentiate infectious from noninfectious virus particles has led to the use of surrogate viruses, like feline calicivirus (FCV) and murine norovirus-1 (MNV), which are propagatable in cell culture. The use of surrogates is predicated on the assumption that they generally mimic the viruses they represent; however, studies are proving this concept invalid. In direct comparisons between FCV and MNV, their susceptibility to temperatures, environmental and food processing conditions, and disinfectants are dramatically different. Differences have also been noted between the inactivation of NoV and its surrogates, thus questioning the validity of surrogates. Considerable research funding is provided globally each year to conduct surrogate studies on NoVs; however, there is little demonstrated benefit derived from these studies in regard to the development of virus inactivation techniques or food processing strategies. Human challenge studies are needed to determine which processing techniques are effective in reducing NoVs in foods. A major obstacle to clinical trials on NoVs is the perception that such trials are too costly and risky, but in reality, there is far more cost and risk in allowing millions of unsuspecting consumers to contract NoV illness each year, when practical interventions are only a few volunteer studies away. A number of clinical trials have been conducted, providing important insights into NoV inactivation. A shift in research priorities from surrogate research to volunteer studies is essential if we are to identify realistic, practical, and scientifically valid processing approaches to improve food safety.
    Food and Environmental Virology 03/2012; 4(1):6-13. DOI:10.1007/s12560-011-9072-7 · 1.98 Impact Factor

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